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Foam cell formation during atherogenesis could be also explained in part by uptake of CRP-opsonized native LDL (193)

It may reach the correct site, but may not be targeted toward the specific agent responsible for oxidative damage, as observed in the case of vitamin E that inhibits lipid peroxidation, but may not prevent the increased oxidative DNA, RNA, and protein damage seen in Alzheimers disease (Pratic, 2008)

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It is a physiologic adaptation of the thyroid gland in response to persistent stimulation by TSH (see Function)